about
Disease-promoting effects of type I interferons in viral, bacterial, and coinfectionsHarnessing alveolar macrophages for sustained mucosal T-cell recall confers long-term protection to mice against lethal influenza challenge without clinical disease.IL-2high tissue-resident T cells in the human liver: Sentinels for hepatotropic infection.Blockade of immunosuppressive cytokines restores NK cell antiviral function in chronic hepatitis B virus infectionTRAIL regulatory receptors constrain human hepatic stellate cell apoptosis.Reference ranges and sources of variability of CD4 counts in HIV-seronegative women and men.Protection or damage: a dual role for the virus-specific cytotoxic T lymphocyte response in hepatitis B and C infection?Licensing virus-specific T cells to secrete the neutrophil attracting chemokine CXCL-8 during hepatitis B virus infectionCD4+ T-lymphocyte telomere length is related to fibrosis stage, clinical outcome and treatment response in chronic hepatitis C virus infectionUpregulation of the Tim-3/galectin-9 pathway of T cell exhaustion in chronic hepatitis B virus infection.The third signal cytokine IL-12 rescues the anti-viral function of exhausted HBV-specific CD8 T cellsDefective natural killer cell anti-viral capacity in paediatric HBV infection.Systemic inflammation and residual viraemia in HIV-positive adults on protease inhibitor monotherapy: a cross-sectional study.Metabolic regulation of hepatitis B immunopathology by myeloid-derived suppressor cells.The level of viral antigen presented by hepatocytes influences CD8 T-cell function.Interferon Alpha Induces Sustained Changes in NK Cell Responsiveness to Hepatitis B Viral Load Suppression In Vivo.Platelets harness the immune response to drive liver cancer.Cytokines induced during chronic hepatitis B virus infection promote a pathway for NK cell-mediated liver damage.IL-10-producing regulatory B cells in the pathogenesis of chronic hepatitis B virus infectionEscaping high viral load exhaustion: CD8 cells with altered tetramer binding in chronic hepatitis B virus infection.Up-regulation of a death receptor renders antiviral T cells susceptible to NK cell-mediated deletion.Functional skewing of the global CD8 T cell population in chronic hepatitis B virus infection.Eomeshi NK Cells in Human Liver Are Long-Lived and Do Not Recirculate but Can Be Replenished from the CirculationT Cells Infiltrating Diseased Liver Express Ligands for the NKG2D Stress Surveillance System.The molecular basis of the failed immune response in chronic HBV: therapeutic implications.Innate and adaptive immune responses in hepatitis B virus infection.The host-pathogen interaction during HBV infection: immunological controversies.Hepatitis B infection: current concepts and future challenges.Living in the liver: hepatic infections.Optimal management of hepatitis B virus infection - EASL Special Conference.The role of innate immunity in the immunopathology and treatment of HBV infection.Liposomal amphotericin B in drug-resistant visceral leishmaniasis.Differential boosting of innate and adaptive antiviral responses during pegylated-interferon-alpha therapy of chronic hepatitis B.Engineering virus-specific T cells that target HBV infected hepatocytes and hepatocellular carcinoma cell lines.CXCR6 marks a novel subset of T-bet(lo)Eomes(hi) natural killer cells residing in human liver.Natural Killer Cells in Liver Disease.Alternative splicing of hepatitis B virus: A novel virus/host interaction altering liver immunity.HBV in 2016: Global and immunotherapeutic insights into hepatitis B.Modulation of the CD8+-T-cell response by CD4+ CD25+ regulatory T cells in patients with hepatitis B virus infectionDistinct Metabolic Requirements of Exhausted and Functional Virus-Specific CD8 T Cells in the Same Host.
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description
researcher ORCID ID = 0000-0001-6384-1462
@en
wetenschapper
@nl
name
Mala K Maini
@ast
Mala K Maini
@en
Mala K Maini
@nl
type
label
Mala K Maini
@ast
Mala K Maini
@en
Mala K Maini
@nl
prefLabel
Mala K Maini
@ast
Mala K Maini
@en
Mala K Maini
@nl
P21
P31
P496
0000-0001-6384-1462